Tomlinson Ian P M, Webb Emily, Carvajal-Carmona Luis, Broderick Peter, Howarth Kimberley, Pittman Alan M, Spain Sarah, Lubbe Steven, Walther Axel, Sullivan Kate, Jaeger Emma, Fielding Sarah, Rowan Andrew, Vijayakrishnan Jayaram, Domingo Enric, Chandler Ian, Kemp Zoe, Qureshi Mobshra, Farrington Susan M, Tenesa Albert, Prendergast James G D, Barnetson Rebecca A, Penegar Steven, Barclay Ella, Wood Wendy, Martin Lynn, Gorman Maggie, Thomas Huw, Peto Julian, Bishop D Timothy, Gray Richard, Maher Eamonn R, Lucassen Anneke, Kerr David, Evans D Gareth R, Schafmayer Clemens, Buch Stephan, Völzke Henry, Hampe Jochen, Schreiber Stefan, John Ulrich, Koessler Thibaud, Pharoah Paul, van Wezel Tom, Morreau Hans, Wijnen Juul T, Hopper John L, Southey Melissa C, Giles Graham G, Severi Gianluca, Castellví-Bel Sergi, Ruiz-Ponte Clara, Carracedo Angel, Castells Antoni, Försti Asta, Hemminki Kari, Vodicka Pavel, Naccarati Alessio, Lipton Lara, Ho Judy W C, Cheng K K, Sham Pak C, Luk J, Agúndez Jose A G, Ladero Jose M, de la Hoya Miguel, Caldés Trinidad, Niittymäki Iina, Tuupanen Sari, Karhu Auli, Aaltonen Lauri, Cazier Jean-Baptiste, Campbell Harry, Dunlop Malcolm G, Houlston Richard S
Molecular and Population Genetics Laboratory, London Research Institute, Cancer Research UK, London WC2A 3PX, UK.
Nat Genet. 2008 May;40(5):623-30. doi: 10.1038/ng.111. Epub 2008 Mar 30.
To identify colorectal cancer (CRC) susceptibility alleles, we conducted a genome-wide association study. In phase 1, we genotyped 550,163 tagSNPs in 940 familial colorectal tumor cases (627 CRC, 313 high-risk adenoma) and 965 controls. In phase 2, we genotyped 42,708 selected SNPs in 2,873 CRC cases and 2,871 controls. In phase 3, we evaluated 11 SNPs showing association at P < 10(-4) in a joint analysis of phases 1 and 2 in 4,287 CRC cases and 3,743 controls. Two SNPs were taken forward to phase 4 genotyping (10,731 CRC cases and 10,961 controls from eight centers). In addition to the previously reported 8q24, 15q13 and 18q21 CRC risk loci, we identified two previously unreported associations: rs10795668, located at 10p14 (P = 2.5 x 10(-13) overall; P = 6.9 x 10(-12) replication), and rs16892766, at 8q23.3 (P = 3.3 x 10(-18) overall; P = 9.6 x 10(-17) replication), which tags a plausible causative gene, EIF3H. These data provide further evidence for the 'common-disease common-variant' model of CRC predisposition.
Cancer Epidemiol Biomarkers Prev. 2009-10-20
Carcinogenesis. 2012-1-10
Cancer Epidemiol Biomarkers Prev. 2010-11-11
Br J Cancer. 2010-7-20
World J Gastrointest Oncol. 2023-3-15
Front Cell Dev Biol. 2022-2-18
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